Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Bach Cuc Nguyen; Karine Lefort; Anna Mandinova; Dario Antonini; Vikram Devgan; Giusy Della Gatta; Maranke I. Koster; Zhuo Zhang; Jian Wang; Alice Tommasi Di Vignano; Jan Kitajewski; Giovanna Chiorino; Dennis R. Roop; Caterina Missero; G. Paolo Dotto

doi:10.1101/gad.1406006

Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Bach Cuc Nguyen, Karine Lefort, Anna Mandinova, Dario Antonini, Vikram Devgan, Giusy Della Gatta, Maranke I. Koster, Zhuo Zhang, Jian Wang, Alice Tommasi Di Vignano, Jan Kitajewski, Giovanna Chiorino, Dennis R. Roop, Caterina Missero, G. Paolo Dotto

IRCCS SDN

Research output: Contribution to journal › Article › peer-review

Abstract

Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation.

Original language	English
Pages (from-to)	1028-1042
Number of pages	15
Journal	Genes and Development
Volume	20
Issue number	8
DOIs	https://doi.org/10.1101/gad.1406006
Publication status	Published - Apr 15 2006

Keywords

HES/HERP family members
Interferon-responsive genes
Keratinocyte
Notch
p63
Stem cells

ASJC Scopus subject areas

Genetics
Developmental Biology

Access to Document

10.1101/gad.1406006

Fingerprint Dive into the research topics of 'Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation'. Together they form a unique fingerprint.

Cite this

Nguyen, B. C., Lefort, K., Mandinova, A., Antonini, D., Devgan, V., Gatta, G. D., Koster, M. I., Zhang, Z., Wang, J., Di Vignano, A. T., Kitajewski, J., Chiorino, G., Roop, D. R., Missero, C., & Dotto, G. P. (2006). Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation. Genes and Development, 20(8), 1028-1042. https://doi.org/10.1101/gad.1406006

Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation. / Nguyen, Bach Cuc; Lefort, Karine; Mandinova, Anna; Antonini, Dario; Devgan, Vikram; Gatta, Giusy Della; Koster, Maranke I.; Zhang, Zhuo; Wang, Jian; Di Vignano, Alice Tommasi; Kitajewski, Jan; Chiorino, Giovanna; Roop, Dennis R.; Missero, Caterina; Dotto, G. Paolo.

In: Genes and Development, Vol. 20, No. 8, 15.04.2006, p. 1028-1042.

Research output: Contribution to journal › Article › peer-review

Nguyen, Bach Cuc ; Lefort, Karine ; Mandinova, Anna ; Antonini, Dario ; Devgan, Vikram ; Gatta, Giusy Della ; Koster, Maranke I. ; Zhang, Zhuo ; Wang, Jian ; Di Vignano, Alice Tommasi ; Kitajewski, Jan ; Chiorino, Giovanna ; Roop, Dennis R. ; Missero, Caterina ; Dotto, G. Paolo. / Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation. In: Genes and Development. 2006 ; Vol. 20, No. 8. pp. 1028-1042.

@article{8b5084dd856b4aa4812f53d56892145e,

title = "Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation",

abstract = "Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation.",

keywords = "HES/HERP family members, Interferon-responsive genes, Keratinocyte, Notch, p63, Stem cells",

author = "Nguyen, {Bach Cuc} and Karine Lefort and Anna Mandinova and Dario Antonini and Vikram Devgan and Gatta, {Giusy Della} and Koster, {Maranke I.} and Zhuo Zhang and Jian Wang and {Di Vignano}, {Alice Tommasi} and Jan Kitajewski and Giovanna Chiorino and Roop, {Dennis R.} and Caterina Missero and Dotto, {G. Paolo}",

year = "2006",

month = apr,

day = "15",

doi = "10.1101/gad.1406006",

language = "English",

volume = "20",

pages = "1028--1042",

journal = "Genes and Development",

issn = "0890-9369",

publisher = "Cold Spring Harbor Laboratory Press",

number = "8",

}

TY - JOUR

T1 - Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

AU - Nguyen, Bach Cuc

AU - Lefort, Karine

AU - Mandinova, Anna

AU - Antonini, Dario

AU - Devgan, Vikram

AU - Gatta, Giusy Della

AU - Koster, Maranke I.

AU - Zhang, Zhuo

AU - Wang, Jian

AU - Di Vignano, Alice Tommasi

AU - Kitajewski, Jan

AU - Chiorino, Giovanna

AU - Roop, Dennis R.

AU - Missero, Caterina

AU - Dotto, G. Paolo

PY - 2006/4/15

Y1 - 2006/4/15

N2 - Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation.

AB - Notch signaling promotes commitment of keratinocytes to differentiation and suppresses tumorigenesis. p63, a p53 family member, has been implicated in establishment of the keratinocyte cell fate and/or maintenance of epithelial self-renewal. Here we show that p63 expression is suppressed by Notch1 activation in both mouse and human keratinocytes through a mechanism independent of cell cycle withdrawal and requiring down-modulation of selected interferon-responsive genes, including IRF7 and/or IRF3. In turn, elevated p63 expression counteracts the ability of Notch1 to restrict growth and promote differentiation. p63 functions as a selective modulator of Notch1-dependent transcription and function, with the Hes-1 gene as one of its direct negative targets. Thus, a complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation.

KW - HES/HERP family members

KW - Interferon-responsive genes

KW - Keratinocyte

KW - Notch

KW - p63

KW - Stem cells

UR - http://www.scopus.com/inward/record.url?scp=33645894992&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33645894992&partnerID=8YFLogxK

U2 - 10.1101/gad.1406006

DO - 10.1101/gad.1406006

M3 - Article

C2 - 16618808

AN - SCOPUS:33645894992

VL - 20

SP - 1028

EP - 1042

JO - Genes and Development

JF - Genes and Development

SN - 0890-9369

IS - 8

ER -

Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Cite this